脑脊液(CSF)的产生原理,总结了正常大脑中液体量和压力的循环和流出以及调节。颅内高压在这些方面的异常,讨论了脑室肥大和脑积水。脑实质具有细胞框架,在中间空间中具有间质液(ISF)。框架应力和间质液压力(ISFP)组合提供的总应力,在允许重力之后,通常等于脑内压力(ICP),总应力梯度太小,无法测量。当实质压靠脑膜时,实质和蛛网膜下腔塌陷的流体压力可能与ICP不同。流体压力梯度确定流体运动。在成年人中,限制脑脊液从蛛网膜下腔流出会产生颅内高压,当CSF体积变化很小时,称为特发性颅内高压(iIH)。iIH中ICP升高伴随静脉窦压升高,虽然哪个是原因,哪个影响尚不清楚。在头骨生长的婴儿中,限制流出导致头部和CSF体积增加。在成年人中,脑室肥大可能是由于脑萎缩或,在脑积水中,颅内脑脊液流动阻塞。在非交通性脑积水中,流经或流出心室的血流被某种方式阻塞,而在交通性脑积水中,阻塞在大脑池和流出的颅骨之间。当正常流出路线受阻时,脑室中持续的CSF产生可能通过脑室周围水肿层和血管周围间隙通过实质流出而部分平衡。在成年人中,继发性脑积水,由于明显的血流阻塞而导致ICP升高。相比之下,在正常压力脑积水(NPH)中看到更微妙的阻塞流,必须在其他地方降低流体压力,例如在一些蛛网膜下腔。特发性NPH,脑室肥大伴有步态障碍,痴呆和/或尿失禁,功能缺陷有时可以通过分流或第三脑室造瘘术来逆转。在晚期脑积水中,实质收缩是不可逆的,伴有细胞框架丧失,但可能不会在早期发生。无论是通过排除流体还是其他方式。概述了解释脑积水发展所需的进一步研究。
The principles of cerebrospinal fluid (CSF) production, circulation and outflow and regulation of fluid volumes and pressures in the normal brain are summarised. Abnormalities in these aspects in intracranial hypertension, ventriculomegaly and hydrocephalus are discussed. The brain parenchyma has a cellular framework with interstitial fluid (ISF) in the intervening spaces. Framework stress and interstitial fluid pressure (ISFP) combined provide the total stress which, after allowing for gravity, normally equals intracerebral pressure (ICP) with gradients of total stress too small to measure. Fluid pressure may differ from ICP in the parenchyma and collapsed subarachnoid spaces when the parenchyma presses against the meninges. Fluid pressure gradients determine fluid movements. In adults, restricting CSF outflow from subarachnoid spaces produces intracranial hypertension which, when CSF volumes change very little, is called idiopathic intracranial hypertension (iIH). Raised ICP in iIH is accompanied by increased venous sinus pressure, though which is cause and which effect is unclear. In infants with growing skulls, restriction in outflow leads to increased head and CSF volumes. In adults, ventriculomegaly can arise due to cerebral atrophy or, in hydrocephalus, to obstructions to intracranial CSF flow. In non-communicating hydrocephalus, flow through or out of the ventricles is somehow obstructed, whereas in communicating hydrocephalus, the obstruction is somewhere between the cisterna magna and cranial sites of outflow. When normal outflow routes are obstructed, continued CSF production in the ventricles may be partially balanced by outflow through the parenchyma via an oedematous periventricular layer and perivascular spaces. In adults, secondary hydrocephalus with raised ICP results from obvious obstructions to flow. By contrast, with the more subtly obstructed flow seen in normal pressure hydrocephalus (NPH), fluid pressure must be reduced elsewhere, e.g. in some subarachnoid spaces. In idiopathic NPH, where ventriculomegaly is accompanied by gait disturbance, dementia and/or urinary incontinence, the functional deficits can sometimes be reversed by shunting or third ventriculostomy. Parenchymal shrinkage is irreversible in late stage hydrocephalus with cellular framework loss but may not occur in early stages, whether by exclusion of fluid or otherwise. Further studies that are needed to explain the development of hydrocephalus are outlined.